|Trade names||Proscar, Propecia, others|
|Synonyms||MK-906; L-652,931; 17β-(N-tert-Butylcarbamoyl)-4-aza-5α-androst-1-en-3-one; N-(1,1-Dimethylethyl)-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide|
|Drug class||5α-Reductase inhibitor|
|Biological half-life||Adults: 5–6 hours
Elderly: >8 hours
|Chemical and physical data|
|Molar mass||372.549 g/mol|
|3D model (JSmol)|
Finasteride, sold under the brand names Proscar and Propecia among others, is a medication used mainly to treat an enlarged prostate or scalp hair loss in men. It can also be used to treat excessive hair growth in women and as a part of hormone therapy for transgender women. It is taken by mouth.
Side effects are generally mild. It may increase the risk of certain rare forms of prostate cancer, and that some men may experience sexual dysfunction, depression, anxiety, or breast enlargement; the sexual dysfunction can be very distressing. Finasteride is a 5α-reductase inhibitor and works by decreasing the production of dihydrotestosterone (DHT), an androgen sex hormone, which makes DHT less available in key tissues like the prostate gland and scalp. It inhibits two of the three forms of 5α-reductase and can decrease DHT levels in the blood by up to 70%.
Finasteride was introduced for the treatment of prostate enlargement in 1992 and was approved for the treatment of scalp hair loss in 1997. It was the first 5α-reductase inhibitor to be introduced and was followed by dutasteride a number of years later. The drug is available as a generic medication.
- 1 Medical uses
- 2 Contraindications
- 3 Adverse effects
- 4 Pharmacology
- 5 Chemistry
- 6 History
- 7 Society and culture
- 8 References
- 9 External links
Physicians sometimes prescribe finasteride for the treatment of benign prostatic hyperplasia (BPH), informally known as an enlarged prostate. Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start of urination, and decreased urinary flow. It provides less symptomatic relief than alpha-1 blockers such as tamsulosin and symptomatic relief is slower in onset (six months or more of treatment with finasteride may be required to determine the therapeutic results of treatment). Symptomatic benefits are mainly seen in those with prostate volume > 40 cm3. In long-term studies finasteride but not alpha-1 inhibitors reduce the risk of acute urinary retention (−57% at 4 years) and the need for surgery (−54% at 4 years). If the drug is discontinued, any therapeutic benefits reverse within about 6–8 months.
A 2010 Cochrane review found a 25–26% reduction in the risk of developing prostate cancer with 5α-reductase inhibitor chemoprevention. However, 5α-reductase inhibitors have been found to increase the risk of developing certain rare but aggressive forms of prostate cancer (27% risk increase), although not all studies have observed this.
Scalp hair loss
Finasteride is sometimes used to treat pattern hair loss (androgenetic alopecia) in men only. Treatment slows further hair loss and provides about 30% improvement in hair loss after six months of treatment, with effectiveness usually only persisting as long as the drug is taken, although on occasion hair loss is slowed indefinitely following withdrawal. Finasteride has also been tested for pattern hair loss in women; the results were no better than placebo.
Excessive hair growth
Finasteride has been found to be effective in the treatment of hirsutism (excessive facial and/or body hair growth) in women. In a study of 89 women with hyperandrogenism due to persistent adrenarche syndrome, finasteride produced a 93% reduction in facial hirsutism and a 73% reduction bodily hirsutism after 2 years of treatment. Other studies using finasteride for hirsutism have also found it to be clearly effective.
Finasteride is sometimes used in hormone replacement therapy for transgender women due to its antiandrogenic effects, in combination with a form of estrogen. However, little clinical research of finasteride use for this purpose has been conducted and evidence of safety or efficacy is limited. Moreover, caution has been recommended when prescribing finasteride to transgender women, as finasteride may be associated with side effects such as depression, anxiety, and suicidal ideation, symptoms that are particularly prevalent in the transgender population and in others at high risk already.
A 2010 Cochrane review concluded that adverse effects from finasteride are rare when used for BPH. A 2017 review of men with BPH found that finasteride resulted in a 45% greater risk of erectile dysfunction and a 54% greater risk of hypoactive sexual desire.
The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade prostate cancer, as the treatment of BPH lowers PSA (prostate-specific antigen), which could mask the development of prostate cancer. Although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not increased, there are post-marketing reports of breast cancer in association with its use. Available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers.
A 2015 meta analysis found that none of the clinical trials testing finasteride in hair loss had adequate safety reporting and did not provide sufficient information to establish the safety profile for finasteride as a treatment for hair loss. The study concluded the existing clinical trials of finasteride for hair loss provide very limited information on toxicity, are of poor quality, and seem to be systematically biased toward under-detection of adverse events. Moreover, the trials submitted to the FDA for approval for hair loss excluded most men who are typically prescribed finasteride for androgenic alopecia.
Finasteride causes short-term sexual dysfunction in some men, which can be very distressing. Whether finasteride causes long-term sexual dysfunction in some men after stopping drug treatment is unclear. There are case reports of persistent diminished libido or erectile dysfunction after stopping the drug and the FDA has updated the label to inform people of these reports. When finasteride was originally approved for hair loss in 1997, the FDA approval review reported that it appears well tolerated, with the most common side effects being related to sexual function. In many people these side effects resolve if the medication is stopped and occasionally resolve even if the medication is continued. They additionally state "the sexual functioning questionnaire seems to have given a sensitive reflection of the disturbance on sexual functioning".
The 2010 Cochrane review found that compared with placebo, men taking finasteride are at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder for the first year of treatment; the rates of these effects became indistinguishable from placebo after 2–4 years and these side effects usually got better over time. Another 2010 review found that when used for hair loss finasteride increased rates of sexual problems. A 2016 review of 5α-reductase inhibitors for prostatic hyperplasia found that sexual dysfunction was 2.5 times more likely in those who used them. Another 2016 review, a meta-analysis found that sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride. This adverse effect has been linked to lower quality of life and can cause stress in relationships. There is also an association with lowered sexual desire. It has been reported that in a subset of men, these adverse sexual side effects may persist even after discontinuation of finasteride or dutasteride.
Finasteride is a 5α-reductase inhibitor, specifically the type II and III isoenzymes. As of 2012, the tissues in which the isoforms of 5α-reductase is expressed were unclear, as different investigators have gotten varying results with different reagents, methods, and tissues examined, but the isoforms appears to widely expressed.
By inhibiting 5α-reductase, finasteride prevents conversion of testosterone to dihydrotestosterone (DHT) by the type II and III isoenzymes, resulting in a decrease in serum DHT levels by about 65 to 70% and in prostate DHT levels by up to 85 to 90%, where expression of the type II isoenzyme predominates. Unlike triple inhibitors of all three isoenzymes of 5α-reductase like dutasteride which can reduce DHT levels in the entire body by more than 99%, finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with more than 100-fold less inhibitory potency for type I as compared to type II (IC50 = 313 nM and 11 nM, respectively).
In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1), although its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than 5α-reductase type I) and hence is unlikely to be of clinical significance.
By inhibiting 5α-reductase and thus preventing DHT production, finasteride reduces androgen activity in tissues like the prostate gland and the scalp. In the prostate, this reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia. Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis. Neurosteroids like 3α-androstanediol and allopregnanolone activate the GABAA receptor in the brain; because finasteride prevents the formation of neurosteroids, it may contribute to a reduction of GABAA activity (see also neurosteroidogenesis inhibitor). Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.
The mean oral bioavailability of finasteride is approximately 65%. Its volume of distribution is 76 L/kg. The plasma protein binding of finasteride is 90%. The drug has been found to cross the blood–brain barrier, whereas levels in semen were found to be undetectable. Finasteride is extensively metabolized in the liver, first by hydroxylation via CYP3A4 and then by aldehyde dehydrogenase. The metabolites of finasteride have about 20% of its potency in inhibiting 5α-reductase and hence its metabolites are not particularly active. The drug has a terminal half-life of 5 to 6 hours in adult men (18–60 years of age) and a terminal half-life of 8 hours or more in elderly men (greater than 70 years of age). It is eliminated as its metabolites 57% in the feces and 40% in the urine.
Finasteride, also known as 17β-(N-tert-butylcarbamoyl)-4-aza-5α-androst-1-en-3-one, is a synthetic androstane steroid and 4-azasteroid. It is an analogue of androgen steroid hormones like testosterone and DHT. As an unconjugated steroid, finasteride is a highly lipophilic compound.
In 1942, James Hamilton observed that prepubertal castration prevents the later development of male pattern baldness in mature men. In 1974, Julianne Imperato-McGinley of Cornell Medical College in New York attended a conference on birth defects. She reported on a group of intersex children in the Caribbean who appeared sexually ambiguous at birth, and were initially raised as girls, but then grew external male genitalia and other masculine characteristic after onset of puberty. Her research group found these children shared a genetic mutation, causing deficiency of the 5α-reductase enzyme and male hormone dihydrotestosterone (DHT), which was found to have been the etiology behind abnormalities in male sexual development. Upon maturation, these individuals were observed to have smaller prostates which were underdeveloped, and were also observed to lack incidence of male pattern baldness.
In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who were suffering from benign prostatic hyperplasia.
Finasteride was developed under the code name MK-906. In 1992, finasteride (5 mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar. In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of MPB, which was marketed under the brand name Propecia.
Society and culture
Finasteride is marketed primarily under the brand names Propecia, for pattern hair loss, and Proscar, for BPH, both of which are products of Merck & Co. There is 1 mg of finasteride in Propecia and 5 mg in Proscar. Merck's patent on finasteride for the treatment of BPH expired on June 19, 2006. Merck was awarded a separate patent for the use of finasteride to treat pattern hair loss. This patent expired in November 2013. Finasteride is also marketed under a variety of other brand names throughout the world.
Men in the U.S. and Canada concerned about persistent sexual side effects "coined the phrase 'post-finasteride syndrome', which they say is characterized by sexual, neurological, hormonal and psychological side effects that can persist in men who have taken finasteride for hair loss or an enlarged prostate". In 2012, a health advocacy group called the Post-Finasteride Syndrome Foundation was formed with the primary goal of finding a cure for the reported syndrome and a secondary goal of raising awareness. According to the company's 1Q2016 financial filing, Merck is a defendant in 1,385 product liability lawsuits which have been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride.
From 2005 to 2009, the World Anti-Doping Agency banned finasteride because it was discovered that the drug could be used to mask steroid abuse. It was removed from the list effective January 1, 2009, after improvements in testing methods made the ban unnecessary. Athletes who used finasteride and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romário and ice hockey goaltender José Théodore.
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[...] caution is recommended while prescribing oral finasteride to male-to-female transsexuals, as the drug has been associated with inducing depression, anxiety and suicidal ideation, symptoms that are particularly common in patients with gender dysphoria, who are already at a high risk.
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